We have used CO2 laser-induced transmyocardial channels to promote direct communications between ventricular blood and myocardial vasculature. This technique is intended to revascularize the ischemic subendocardium associated with left ventricular hypertrophy. To date, no studies have quantitatively analyzed the laser technique to increase subendocardial perfusion. Furthermore, no studies have examined the condition in which transmyocardial revascularization would be most likely and appropriately applied, i.e., in the hypertrophied heart. In the hypertrophied heart, the coronary arteries are structurally normal. Those techniques attempting to increase perfusion by restoring coronary structure are of little value in remedying the subendocardial ischemia associated with the hypertrophied heart. Finally, present evidence documenting potential myocardial damage created by the laser is lacking. We, therefore, set out to establish the stated hypotheses: 1. Transmyocardial revascularization with the CO2 laser will increase endocardial perfusion in the hypertrophied left ventricle. 2. The clinical advantage of increased endocardial perfusion will outweigh the potential disadvantage of damaged myocardium due to laser surgery. Using radioactive microspheres, myocardial perfusion will be measured in cardiac tissue with laser-induced transmyocardial channels. These measurements will be compared with cardiac tissue lacking such channels. Evidence of revascularization provided by microsphere data will be supported by transmural electrogram tracings. Decreased amplitudes and delayed time-to-onset values, associated with the ischemic subendocardium of the hypertrophied heart, will return to normal values after transmyocardial revascularization. Transmyocardial channel patency and continuity of the myocardial vasculature with these channels will be documented using cine-angiography and post-mortem myocardial microvascular corrosion casts. Finally, potential damage to the myocardium created by the CO2 laser, will be quantified. Regional cardiac mechanics of the lasered myocardium, as measured with piezoelectric ultrasound transducers, will be compared to those of the non-lasered myocardium. Collected data will be analyzed by two-way analysis of variance, multi-way analysis of variance, and pair-wise comparisons using Scheffe's procedure. If the stated hypotheses prove to be verified, transmyocardial revascularization with the CO2 laser may become a valuable technique for reducing subendocardial ischemia associated with left ventricular hypertrophy.